Impaired sympathetic nerve function in the inflamed rat intestine

Gastroenterology. 1991 Mar;100(3):675-82. doi: 10.1016/0016-5085(91)80011-w.

Abstract

The effect of intestinal inflammation on norepinephrine release from the myenteric plexus in the Trichinella spiralis-infected rat was assessed. Longitudinal muscle-myenteric plexus preparations were preincubated with [3H]norepinephrine and release was evoked by electrical field stimulation and KCl administration. Preincubation of preparations with desipramine or pretreatment of rats with 6-hydroxydopamine significantly suppressed the uptake and evoked release of [3H]norepinephrine; electrical field stimulation but not KCl-evoked release of [3H] norepinephrine was sensitive to tetrodotoxin. These results confirm the presence of functioning sympathetic nerves in the preparations. T. spiralis infection was associated with significant suppression of both electrical field stimulation and KCl-evoked release of [3H]norepinephrine on the sixth day postinfection, and the suppression persisted 100 days postinfection. No suppression of [3H]norepinephrine release was seen in the worm-free and noninflamed ileum of infected rats. Suppression of [3H]norepinephrine release from the jejunum of infected rats was attenuated by treatment with betamethasone (3.0 mg/kg SC daily). These results are consistent with the hypothesis that intestinal inflammation suppresses the release of norepinephrine from the myenteric plexus in the Trichinella-infected rat.

MeSH terms

  • Animals
  • Betamethasone / pharmacology
  • Betamethasone / therapeutic use
  • Ileum / metabolism
  • Inflammation / drug therapy
  • Inflammation / physiopathology
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism*
  • Jejunum / metabolism
  • Male
  • Norepinephrine / metabolism*
  • Peroxidase / drug effects
  • Peroxidase / metabolism
  • Rats
  • Rats, Inbred Strains
  • Sympathetic Nervous System / drug effects
  • Sympathetic Nervous System / physiopathology*
  • Trichinella*
  • Trichinellosis / physiopathology*

Substances

  • Betamethasone
  • Peroxidase
  • Norepinephrine